Relish plays a dynamic role in the niche to modulate Drosophila blood progenitor homeostasis in development and infection.
Parvathy RameshNidhi Sharma DeyAditya KanwalSudip MandalLolitika MandalPublished in: eLife (2021)
Immune challenges demand the gearing up of basal hematopoiesis to combat infection. Little is known about how during development, this switch is achieved to take care of the insult. Here, we show that the hematopoietic niche of the larval lymph gland of Drosophila senses immune challenge and reacts to it quickly through the nuclear factor-κB (NF-κB), Relish, a component of the immune deficiency (Imd) pathway. During development, Relish is triggered by ecdysone signaling in the hematopoietic niche to maintain the blood progenitors. Loss of Relish causes an alteration in the cytoskeletal architecture of the niche cells in a Jun Kinase-dependent manner, resulting in the trapping of Hh implicated in progenitor maintenance. Notably, during infection, downregulation of Relish in the niche tilts the maintenance program toward precocious differentiation, thereby bolstering the cellular arm of the immune response.
Keyphrases
- nuclear factor
- immune response
- toll like receptor
- signaling pathway
- quality improvement
- bone marrow
- induced apoptosis
- cell proliferation
- cell cycle arrest
- pi k akt
- dendritic cells
- tyrosine kinase
- inflammatory response
- lps induced
- aedes aegypti
- chronic pain
- drosophila melanogaster
- cell fate
- hematopoietic stem cell
- pluripotent stem cells